ANAPHYLAXIS Flashcards
RED FLAGS
DIFFERENTIALS
- Asthma
- Hyperventilation
- Vasovagal response
- PE
- Foreign body
- Airway obstruction
DEFINITION
Anaphylaxis is a severe life-threatening systemic/generalised hypersensitivity reaction characterised by A/B/C problems with or without skin or mucosal changes.
RISK FACTORS
- Modifiable: diet, lifestyle, smoking, alcohol, stimulant use, hyperlipidaemia, hypertension.
- Non-modifiable: age, gender, family Hx, race, congenital cholesterol disorders.
PATHOPHYSIOLOGY
Anaphylaxis results from an exaggerated IgE-mediated reaction post-exposure to an antigen.
- 1st exposure: macrophage digests allergen –> presents antigen to T helper cell –> causes B lymphocyte to turn into a plasma cell –> secrete IgE (immunoglobin) antibodies –> IgE moves into tissue & vasculature –> occupy receptors on mast cells & basophils (now sensitised)
- 2nd exposure: mast cell & basophil degranulate (cytokines, primarily histamine) –> more cytokine production –> allergic symptoms + more recruitment of inflammatory mediators .
Vascular smooth muscle relaxes, resulting in a drop in BP. Smooth venous circulatory muscles also relax, causing blood to pool –> reducing venous return to the heart with a consequent reduction in CO2. The antigen-antibody reaction also causes bronchoconstriction in the lungs + increased vascular permeability in the laryngeal mucosa, resulting in oedema.
Biphasic reaction: anaphylaxis reaction can return after symptoms have resolved despite not having another exposure to the allergen.
TYPES
- Immunologic: IgE mediated mast cell & basophil degranulation.
- Non-immunologic: not mediated by IgE but form some other cause that triggers mast cell & basophil degranulation directly
MANISFESTATIONS
- CV: increased HR that can decompensate to bradycardia, flushing, headache, vasodilation, increased cellular permeability –> hypotension –> arrhythmias & ischemia. Clotting & lysis –> DIC.
- Resp: bronchospasm, rhinorrhoea, oropharyngeal angioedema, wheeze, pulmonary hyperinflation, oedema, mucus plugging, resp. failure & arrest.
- GIT: histamine increased abdominal contraction & acid production –> nausea/vomiting
- CUT: pruritis, urticaria, pallor & hypoperfusion can hide urticaria.
TREATMENT
Primary survey
- D: remove allergen.
- R:
- A: advanced airway.
- B: O2.
- C: IV access.
- D (drugs): IM adrenaline, NEB Salbutamol/Ipratropium bromide/Adrenaline, IV fluids + Hydrocortisone + Glucagon.
- E: expose, H-T. Position supine to maintain cerebral perfusion when hypotensive. R&R.
Secondary Survey
- Thorough NSA, CVA, & RSA, reassessments.
SITREP
- CCP: IV Adrenaline/Salbutamol, advanced airway/intubation.
- ACP: extra hands for decompensation.
PARAMEDIC ROLE
Role of paramedics
- Continue paramedic management & monitor for biphasic reaction.
PHARMACOLOGY
Adrenaline
A naturally occurring catecholamine which acts on α- & ß-adrenergic receptors. It is the 1st line therapy for anaphylaxis.
- α1: vasoconstriction, increases vascular permeability (which can cause the loss of intravascular fluid volume & hypotension), reduces oropharyngeal angioedema.
- ß1: increase HR (chronotropy), increase myocardial contraction (inotropy), increase ventricular irritability, vasoconstriction in skin & mucosa.
- ß2: smooth muscle relaxant (bronchodilation), enhances inspiration +lung capacity, & inhibits inflammatory mediator release.
Adrenaline binds to specific receptors on immune cells which helps to suppress histamine release (responsible for allergic reactions). It also produces an increase in blood sugar & glycogenolysis in the liver.
- Side effects: anxiety, hypertension, palpitations, pupil dilation, tremor.
DEFINITIVE CARE
- Antihistamine: in hospital for urticaria, not 1st line treatment.
- Other: Adrenaline injector administration/training, develop ASCIA anaphylaxis action plan.
- Referral to an allergist: Confirm the cause by pinprick allergen testing.
